Avid Bioservices Inc (CDMO)

[biopharm]

JBainseky, great question! Dmitry Gabrilovich has answsers... and I have been wondering about that slide from the very beginning, in combination with slide #38 of 45.

CJ's post of Dr. Brekkens slides:
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=99937160

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I've written many posts in the past re: Notch Signaling and "all" complexities within this pathway takes on a chain reaction so to speak and PS targeting I say is what they are seeing that is initiating all these chain reactions "for the better" in many indications.

I'll make a bold claim right now, after looking through probably a hundred publications that mention IFNy (Interferon Gamma) and its relation to diabetes. I'll toss out a couple of the links below and have no time now but will try to organize a bunch of them that "may" show this is what Peregrine and KOL's are working towards re: progress in auto-immune diseases...

Interferon gamma (IFN-?) disrupts energy expenditure and metabolic homeostasis by suppressing SIRT1 transcription

2011

Therefore, our data delineate an IFN-?/HIC1/CIITA axis that contributes to metabolic dysfunction by suppressing SIRT1 transcription in skeletal muscle cells and as such shed new light on the development of novel therapeutic strategies against type 2 diabetes.

Mounting evidence connects chronic inflammation to the disruption of cellular metabolism (17). Liu et al. have recently reported that mast cells contribute to the pathogenesis of type 2 diabetes by producing the pro-inflammatory cytokine interferon gamma (IFN-?) (18). Several independent investigations have implicated IFN-y in a host of disorders associated with mitochondrial defect. IFN-?, through its downstream mediator JAK/IRF-1, disturbs the mitochondrial membrane potential and exacerbates liver injury induced by LPS (19). IFN-? also desensitizes adipocyte to insulin and blocks the maturation of pre-adipocyte in a JAK1/STAT1 dependent manner (20). Here we report that IFN-? down-regulates SIRT1 transcription and impairs energy expenditure in skeletal muscle cells by inducing the transcriptional modulators class II transactivator (CIITA) and hypermethylated in cancer 1 (HIC1). Our data highlight a previously unknown function for CIITA/HIC1 complex and provide novel insight into the pathogenesis of type 2 diabetes.

Results:

IFN-? disrupts metabolic homeostasis

Mast cell-derived IFN-? triggers inflammatory responses and contributes to the pathogenesis of type 2 diabetes

http://nar.oxfordjournals.org/content/early/2011/11/07/nar.gkr984.full

Critical role for IFN-gamma in natural killer cell-mediated protection from diabetes.

2008

Our findings demonstrate that NK cells mediate the protective effects of CFA through secretion of IFN-gamma.

http://www.ncbi.nlm.nih.gov/pubmed/18085661

Now, "Judith Klein-Seetharaman" has worked with Dmitry Gabrilovich... and link below just to verify her work:

Oxidized Lipids Block Antigen Cross-Presentation by Dendritic Cells in Cancer.

Wei Cao, Rupal Ramakrishnan, Vladimir A Tuyrin, Filippo Veglia, Thomas Condamine, Andrew Amoscato, Dariush Mohammadyani, Joseph J Johnson, Lan Min Zhang, Judith Klein-Seetharaman, Esteban Celis, Valerian E Kagan, Dmitry I Gabrilovich

The Journal of Immunology

http://www.researchgate.net/publication/260272570_Oxidized_Lipids_Block_Antigen_Cross-Presentation_by_Dendritic_Cells_in_Cancer

Judith Klein

Insulin and IFN gamma receptor studies, Funded by: MATERIA MEDICA, Project Start Date: 01/11/2013 Project End Date: 31/12/2014

http://www2.warwick.ac.uk/fac/med/staff/jklein/

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The Journal of Immunology

.... take a look at all the titles but this one I'll point out specifically below:

VOL. 192 | NO. 6 | March 15, 2014 | Pages 2527–2934

CUTTINGEDGE

2537 Cutting Edge:

IFN-gR Signaling in Non–T Cell Targets Regulates T Cell–Mediated Intestinal Inflammation through Multiple Mechanisms

Jeong-su Do, Kewal Asosingh, William M. Baldwin, III, and Booki Min


2576 The DC-HIL/Syndecan-4 Pathway Regulates Autoimmune Responses through Myeloid-Derived Suppressor Cells

Jin-Sung Chung, Kyoichi Tamura, Hideo Akiyoshi, Ponciano D. Cruz, Jr., and Kiyoshi Ariizumi

http://www.jimmunol.org/content/192/6.toc.pdf

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There are way too many other publications sources, some which may be better suited to made a good case that PS targeting ( as we know influences MDSC's..etc) and just may be that doorway to the immediate beginning of hundreds of trials/collaborations..etc en route to solutions for the hundreds of auto-immune diseases...

I still do not believe we have seen (as volgoat has mentioned a few times as well)--- the true reasons just yet why we picked up 4 key KOL's--- one being Dmitry Gabrilovich, who happens to be speaking all over the place:

May 2, 2014

Pitt Immunology Symposium

Distinguished speakers, AM session

Dmitry Gabrilovich, MD/PhD, Wistar Institute
Distinguished Guest - Mechanisms Regulating Differentiation and Function of Myeloid-Derived Suppressor Cells in Cancer

http://www.2014immunology.pitt.edu/

So PS Targeting to MDSC changes to IFNy (Interferon Gamma) that has been proven in dozens of publications to have a correlation, but before the MOA of PS targeting was "better understood" and this better understanding has not been fully disclosedas of yet by Peregrine. Probably using it for leverage I'd say against Big Pharma and to make a deal of a lifetime, because PS targeting is needed for just about everything... including diabetes I believe.